Tell me, It is wrong on Infection?

Coronavirus entry point[edit]
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As a transmembrane protein, ACE2 serves as the main entry point into cells for some coronaviruses, including HCoV-NL63,[5] SARS-CoV (the virus that causes SARS),[23][24][25] and SARS-CoV-2[26] (the virus that causes COVID-19).[27][28][29] More specifically, the binding of the spike S1 protein of SARS-CoV and SARS-CoV2 to the enzymatic domain of ACE2 on the surface of cells results in endocytosis and translocation of both the virus and the enzyme into endosomes located within cells.[30][31] This entry process also requires priming of the S protein by the host serine protease TMPRSS2, the inhibition of which is under current investigation as a potential therapeutic.[32]

This has led some to hypothesize that decreasing the levels of ACE2, in cells, might help in fighting the infection. On the other hand, ACE2 has been shown to have a protective effect against virus-induced lung injury by increasing the production of the vasodilator angiotensin 1–7.[33] Furthermore, according to studies conducted on mice, the interaction of the spike protein of the coronavirus with ACE2 induces a drop in the levels of ACE2 in cells through internalization and degradation of the protein and hence may contribute to lung damage.[33][34]
https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2
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The above quote can be important for better understanding of potential drugs.
 
Key Proteins and Their Roles in Viral Infection
Identification of targets is important for identifying drugs with high target specificity and/or uncovering existing drugs that could be repurposed to treat SARS-CoV-2 infection. Table2 lists potential targets, their roles in viral infection, and representative existing drugs or drug candidates that reportedly act on the corresponding targets in similar viruses and thus are to be assessed for their effects on SARS-CoV-2 infection...
Conceivably, the interaction of viral S protein with its receptor ACE2 on host cells, and subsequent viral endocytosis into the cells, may also be a viable drug target. For example, the broad-spectrum antiviral drug Arbidol, which functions as a virus-host cell fusion inhibitor to prevent viral entry into host cells against influenza virus,(20) has entered into a clinical trial for treatment of SARS-CoV-2.(21,22) The protease TMPRSS2 produced by the host cells plays an important role in proteolytic processing of S protein priming to the receptor ACE2 binding in human cells.(11) It has been shown that camostat mesylate, a clinically approved TMPRSS2 inhibitor, was able to block SARS-CoV-2 entry to human cells, indicating its potential as a drug for COVID-19
https://pubs.acs.org/doi/10.1021/acscentsci.0c00272
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The above quote also seems to be very interesting to target at basic level and may cover all variants of this infection.
 
[ Although, it is bit odd to mention it in Science forum, but there seems to be some indications which may suggest, it is somewhat natural forces oriented to balance itself on extremes. So we become ideal inspite apparance]. Sorry. Unquote.
 
KUMAR5 said:
Some new body areas defined.
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Indeed. The most interesting feature of SARS-CoV-2 is the neurological aspect of the infection. There are multiple neurological symptoms, the worst of which (in the most serious cases) is the suppression of spontaneous breathing reflex requiring treatment with a positive pressure ventilator. On their own these symptoms indicate that SARS-CoV-2 can cross the BBB, and there are growing reports of the virus being detected in CSF.
 
KUMAR5 said:
Best wishes.
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i am not a micro biologist(or an immunologist[thats an actual doctor type person who is a fully qualified doctor & specializes in immunology, not some american quak-ism for prey the gay away types] but i occasionally chat with some

i think your best wishes may be the only scientifically sound application for discussion

despite the 'best wishes' of many
it appears the immune response to produce anti bodies "appears" to stop at around 3 months
"if" this is true
then best wish is about all you can have
defining the difference between immune systems in people that do not contract a virus
equally to those whom contract it but appear some what a-symptomatic
is not a clear water and oil situation to define.
otherwise they would be putting out vaccines for covid like a canning factory the american economy would not be in free fall

KUMAR5 said:
immunological memory
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is like saying "the pointy stick with the thing on the end"
when you are referring to the gear stick in a manual car heading toward a corner you must change down a gear to survive the exit of.

the immune system is over activated by covid 19 and goes on full throttle until it kills the host

soo
you mean memory to memories an immune response to not produce an allergic response ?

if you see my point

there is no public media i have seen so far that comes from "actual Doctors" that says they have found out why some peoples immune system triggers to over load(the effective fatal part of covid to the majority not counting co-morbidity)

i get your general question.... almost
but you appear to be thinking pictorially(2D) about something that is more 3 dimensional and multi dimensional

explain your question with more of your thinking
more words instead of less words
 
Hercules Rockefeller said:
anyone potentially
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i was americanising my response because in American women are not considered people
they cant just go to hospital and get treatment

pregnancy medical needs is seen in the usa as a political subject to play with
instead of a womens health basic need

so ...
men do not get pregnant
specifically in the usa where womens contraceptive pill used by children teens and adults to control bleeding cramps and other life long health issues
quite aside from its pregnancy contraceptive effect
is viewed as a mens game of politics to play with young girls, teens & womens lifes

soo ..
its not really "anyone" unless EVERYONE has universal health care

not to mention the cost exclusion factor of private health care morality
 
RainbowSingularity said:
despite the 'best wishes' of many
it appears the immune response to produce anti bodies "appears" to stop at around 3 months
"if" this is true
then best wish is about all you can have
defining the difference between immune systems in people that do not contract a virus
equally to those whom contract it but appear some what a-symptomatic
is not a clear water and oil situation to define.
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How both above happen?

Does it suggest that this virus has both friend and foe component which confuse to immune
system for to do full immune response or not?

Friendly Viruses also exist. Why it can not be possible that this virus is a mutated virgin(natural or lab made) of some friendly virus against which immune system is not sufficiently developed in confusion? As such it is friendly outside but inimical inside like a sweet fruit with toxic seeds. Like cancer cells.


the immune system is over activated by covid 19 and goes on full throttle until it kills the host

soo
you mean memory to memories an immune response to not produce an allergic response ?

if you see my point

there is no public media i have seen so far that comes from "actual Doctors" that says they have found out why some peoples immune system triggers to over load(the effective fatal part of covid to the majority not counting co-morbidity)
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I raised one question in this thread previously.

Why, at first, host body cells allow this virus to infect them? I think Virus entry is a cellular
control process then how it happen?

Does this virus present friendly entity to cells or do fatty envelop or protein cuspid of this virus
is somewhat like a nutrient for host cells who therefore allow or welcome it?
 
you appear to be using a text translator to read & write with
this changes the meaning of some technical words and makes discussion more difficult


KUMAR5 said:
Why, at first, host body cells allow this virus to infect them?
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https://coronavirusexplained.ukri.org/en/article/cad0010/

Corona-viruses have three main activities: to deliver genetic instructions in the form of RNA across the membrane of uninfected human cells, to allow newly-made RNA to escape from an infected cell, and to protect the RNA during its journey to discover new, uninfected cells. The RNA of the new coronavirus SARS-CoV-2 is contained within an envelope – an outer fatty membrane. Three viral proteins, called spike, membrane, and envelope are embedded in this outer membrane, and give the virus its distinctive shape and structure. Inside the virus particle the RNA is tightly coiled and coated by a fourth, nucleocapsid protein.
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translation of words that mean
attach to
comes from
changes from
changes to
can be lost in text translators

when technical words are added and common language is used inside that
you easily get 3 layers of wrong/bad text
this makes discussion very difficult

KUMAR5 said:
Does this virus present friendly entity to cells or do fatty envelop or protein cuspid of this virus
is somewhat like a nutrient for host cells who therefore allow or welcome it?
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this information is freely and widely available on the internet

you appear to be attempting to discuss things that are news web site head lines
and then argue if they are scientifically correct

that is called
Gossip
Urban myths
miss information
conspiracy theories
 
RainbowSingularity said:
you appear to be using a text translator to read & write with
this changes the meaning of some technical words and makes discussion more difficult




https://coronavirusexplained.ukri.org/en/article/cad0010/



translation of words that mean
attach to
comes from
changes from
changes to
can be lost in text translators

when technical words are added and common language is used inside that
you easily get 3 layers of wrong/bad text
this makes discussion very difficult



this information is freely and widely available on the internet

you appear to be attempting to discuss things that are news web site head lines
and then argue if they are scientifically correct

that is called
Gossip
Urban myths
miss information
conspiracy theories
Click to expand...
Okay, look at these;
https://insidehpc.com/2020/06/front...ecular-sugar-coating-for-spreading-infection/
[17/07, 5:31 am] A virus uses camouflage to trick the cell. Its capsid or receptor proteins look like nutrients the cell needs. When the virus receptor binds to the cell receptor, the cell thinks the virus is a nutrient, and pulls it in. Now the cell is infected!
https://askabiologist.asu.edu/virus#:~:text=A virus uses camouflage to,Now the cell is infected!
[17/07, 6:17 am] https://insidehpc.com/2020/06/front...ecular-sugar-coating-for-spreading-infection/
 
KUMAR5 said:
Okay, look at these;
https://insidehpc.com/2020/06/front...ecular-sugar-coating-for-spreading-infection/
[17/07, 5:31 am] A virus uses camouflage to trick the cell. Its capsid or receptor proteins look like nutrients the cell needs. When the virus receptor binds to the cell receptor, the cell thinks the virus is a nutrient, and pulls it in. Now the cell is infected!
https://askabiologist.asu.edu/virus#:~:text=A virus uses camouflage to,Now the cell is infected!
[17/07, 6:17 am] https://insidehpc.com/2020/06/front...ecular-sugar-coating-for-spreading-infection/
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These links seem to be advertising puffery, for the makers of a supercomputer, which tell us nothing about the virus.
 
KUMAR5 said:
A virus uses camouflage to trick the cell. Its capsid or receptor proteins look like nutrients the cell needs. When the virus receptor binds to the cell receptor, the cell thinks the virus is a nutrient, and pulls it in. Now the cell is infected!
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Instead on trying to control the behavior of viruses which readily mutate anyway, why not trick the cell to NOT allow the virus to bind to the cell?

The virus triggers cell division via the mitotic mechanism. The mitotic mechanism makes a copy of the original cell including the virus. If we destroy the cells mitotic (MTOC) centers, the cell cannot divide and dies, killing the virus in the process.

An option might be to make the cell "deaf" to the virus' attemps to bind and the virus will just die without doing any harm.

Any knowledgeable comments?
 
Write4U said:
Instead on trying to control the behavior of viruses which readily mutate anyway, why not trick the cell to NOT allow the virus to bind to the cell?

The virus triggers cell division via the mitotic mechanism. The mitotic mechanism makes a copy of the original cell including the virus. If we destroy the cells mitotic (MTOC) centers, the cell cannot divide and dies, killing the virus in the process.

An option might be to make the cell "deaf" to the virus' attemps to bind and the virus will just die without doing any harm.

Any knowledgeable comments?
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Please refer my previous posts for it.
 
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